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There is a paucity of intervention studies investigating nutritional status and associated risk for persons with SCI. Many descriptive and observational publications address the risk for obesity, dyslipidemia and cardiovascular disease, impaired glycemic control and diabetes mellitus. Blood lipid profiles and indicators of impaired glucose tolerance and hyperinsulinemia of persons with SCI have been compared with those of non-SCI controls. Despite the high risk for CVD morbidity and mortality in individuals with SCI as evidenced by blood values, metabolic and lifestyle factors, few studies have addressed the benefits of risk reduction interventions aimed at modifiable factors and have been limited to exercise. Other studies have investigated vitamin and mineral status of persons with SCI and compared values to those of non-SCI controls or to general population norms and have found lower levels of a variety of nutrients in the SCI population. Few publications have suggested screening and supplementation strategies to address these trends.

There is level 5 evidence (from one observational study; Sabour et al. 2016) that elevated protein intake can lower bone mineral densities in individuals with SCI.

There is level 5 evidence (from two observational studies; Tsunoda et al. 2015; Lieberman et al. 2014) that consumption of whole grains, vegetables, fruits and dairy products are important in maintaining adequate dietary intake.

There is level 5 evidence (from two observational studies; Pellicane et al. 2013; Sabour et al. 2012) that age and gender, but not level of injury, predict total caloric intake in individuals with SCI; further, level 5 evidence (from one observational study; Gorgey et al. 2015) suggests that individuals with chronic SCI often have a negative energy balance, consuming fewer calories than they burn.

There is level 5 evidence (from two observational studies; Wong et al. 2014; Wong et al. 2012) that individuals with SCI are at a significant risk for malnutrition and are at risk of worse clinical outcomes in the first year after injury.

There is level 5 evidence (from several observational studies; Chaw et al. 2012, Shem et al. 2012, Shem et al. 2012b, Shem et al. 2011, Seidl et al. 2010, Abel, Ruf & Spahn 2004, Kirshblum et al. 1999) that VFSS and BSE are adequate measures of diagnosing dysphagia in a SCI population.

There is level 5 evidence (from four observational studies; Chaw et al. 2012, Shem et al. 2012, Shem et al. 2012b, Shem et al. 2011) that VFSS and BSE are comparable in diagnosing dysphagia in a SCI population.

There is level 5 evidence (from one observational study: Wolf and Meiers 2003) that FEES is an adequate tool to diagnose dysphagia and monitor treatment progress in a SCI population.

There is level 5 evidence (from several observational studies; Hayashi et al. 2017, Chaw et al. 2012, Shem et al. 2012, Shem et al. 2012b, Shem et al. 2011, Shin et al. 2011, Seidl et al. 2010, Shem et al. 2004, Abel, Ruf & Spahn 2004, Brady et al. 2004 Kirshblum et al. 1999) that presence of a tracheostomy is a risk factor for dysphagia in individuals with SCI.

There is level 5 evidence (from six observational studies; Chaw et al. 2012, Shem et al. 2012, Shem et al. 2012b, Shem et al. 2011, Seidl et al. 2010, Shem et al. 2004) that ventilator use is a risk factor for dysphagia in individuals with SCI.

There is level 5 evidence (from six observational studies; Hayashi et al. 2017, Shem et al. 2012, Shem et al. 2012b, Shem et al. 2011, Shin et al. 2011, Kirshblum et al. 1999) that increasing age is a risk factor for dysphagia in individuals with SCI.

There is level 5 evidence (from four observational studies; Chaw et al. 2012, Shem et al. 2012, Shem et al. 2012b, Shem et al. 2011) that presence of nasogastric tubes are a risk factor for dysphagia in individuals with SCI.

There is level 2 evidence (from one prospective controlled trial and one cohort study; Bennegard & Karlsson 2008; Bauman & Spungen 1994) that glucose uptake is higher in SCI individuals compared to non-SCI individuals.

There is level 2 evidence (from one cohort study and one pre-post study; Bauman & Spungen 1994; Bauman et al. 1999) that SCI individuals with tetraplegia have higher rates of altered glucose metabolism than other SCI individuals.

There is level 2 evidence (from one prospective controlled trial; Ketover et al. 1996) that diabetic and obese SCI individuals show impaired gallbladder emptying in response to a high fat meal compared to healthy SCI individuals.

There is level 1b evidence (from one RCT; Gorgey et al. 2012 and onee pre-post study; Chen et al. 2006) that an intervention program combining diet and exercise is effective for reducing weight among overweight persons with SCI.

There is level 1b evidence (from one RCT; Zemper et al. 2003) that improved health-related behaviours are adopted following a holistic wellness program for individuals with SCI.

There is level 4 evidence (from one pre-post study; Liusuwan et al. 2007) that an education program combining nutrition, exercise and behaviour modification is effective in increasing whole body lean tissue, maximum power output, work efficiency, resting oxygen uptake and shoulder strength in persons with SCI.

There is level 5 evidence (from one observational study; Hata et al. 2016) that social participation and social support have beneficial effects on an individual with SCI’s self-rated health and dietary satisfaction.

There is level 2 evidence (from one prospective controlled trial; Szlachic et al. 2001) that standard dietary counseling (total fat<30% of kcal, saturated fat<10% of kcal, cholesterol<300 mg, carbohydrate 60% of kcal) can reduce total and low density lipoprotein cholesterol among individuals with SCI who have total initial cholesterol >5.2 mmol/L.

There is level 4 evidence (from one pre-post study; Javierre et al. 2005) that daily supplementation with DHA (1.5 g) and EPA (0.75 g) increases plasma DHA and EPA levels but does not alter total cholesterol, very low-, low-, or high-density lipoprotein, triglycerides, or glucose.

There is level 4 evidence (from one pre-post study; Javierre et al. 2006) that DHA and EPA supplementation increases upper body strength and endurance in persons with SCI.

There is level 4 evidence (from one pre-post study; Bauman et al. 2005) that vitamin D supplementation raises serum 25(OH) D levels in persons with chronic SCI. However, the dose and duration required to ensure vitamin D sufficiency remains unclear.

There is level 1a evidence (from one RCT; Kendall et al. 2005) that creatine supplementation did not result in improvements in wrist extensor strength or muscle function.

There is level 1a evidence (from one RCT cross-over trial; Jacobs et al. 2002) that creatine supplementation enhances exercise capacity in persons with complete tetraplegia and may promote greater exercise training benefits.

There is level 2 evidence (from one prospective controlled trial; Baliga et al. 1997) that consumption of a standard liquid meal does not change blood pressure, heart rate or noradrenalin levels in individuals with tetraplegia and postural hypotension.

There is level 2 evidence (from one RCT cross-over trial; Nash et al. 2007) that the consumption of a whey protein plus carbohydrate supplement following fatiguing ambulation improves subsequent ambulation by increasing distance, time to fatigue and caloric expenditure in persons with incomplete SCI.

There is level 3 evidence (from one prospective controlled trial; Asknes et al. 1993) that nutrient-induced thermogenesis is not decreased in individuals with tetraplegia with low sympathoadrenal activity; efferent sympathoadrenal stimulation from the brain is not necessary for nutrient-induced thermogenesis.

There is level 3 evidence (from one case control study; Sutters et al. 1992) that sympathetic control of the kidney is not required for renal sodium conservation in response to dietary salt restriction.